This blog is about statistics, evolution, nutrition, lifestyle, and health issues. A combination of these issues. The focus is on quantitative research and how it can be applied in practice. But you may see other types of posts here (e.g., recipes, ideas, concepts, theories) from time to time.

Monday, October 15, 2012

Obesity rates have increased in the USA over the years, but the steep increase starting around the 1980s is unusual. Wang and Beydoun do a good job at discussing this puzzling phenomenon (), and a blog post by Discover Magazine provides a graph (see below) that clear illustrates it ().

What is the reason for this?

You may be tempted to point at increases in calorie intake and/or changes in macronutrient composition, but neither can explain this sharp increase in obesity in the 1980s. The differences in calorie intake and macronutrient composition are simply not large enough to fully account for such a steep increase. And the data is actually full of oddities.

For example, an article by Austin and colleagues (which ironically blames calorie consumption for the obesity epidemic) suggests that obese men in a NHANES (2005–2006) sample consumed only 2.2 percent more calories per day on average than normal weight men in a NHANES I (1971–1975) sample ().

So, what could be the main reason for the steep increase in obesity prevalence since the 1980s?

The first clue comes from an interesting observation. If you age-adjust obesity trends (by controlling for age), you end up with a much less steep increase. The steep increase in the graph above is based on raw, unadjusted numbers. There is a higher prevalence of obesity among older people (no surprise here). And older people are people that have survived longer than younger people. (Don’t be too quick to say “duh” just yet.)

This age-obesity connection also reflects an interesting difference between humans living “in the wild” and those who do not, which becomes more striking when we compare hunter-gatherers with modern urbanites. Adult hunter-gatherers, unlike modern urbanites, do not gain weight as they age; they actually lose weight (, ).

Modern urbanites gain a significant amount of weight, usually as body fat, particularly after age 40. The table below, from an article by Flegal and colleagues, illustrates this pattern quite clearly (). Obesity prevalence tends to be highest between ages 40-59 in men; and this has been happening since the 1960s, with the exception of the most recent period listed (1999-2000).

In the 1999-2000 period obesity prevalence in men peaked in the 60-74 age range. Why? With progress in medicine, it is likely that more obese people in that age range survived (however miserably) in the 1999-2000 period. Obesity prevalence overall tends to be highest between ages 40-74 in women, which is a wider range than in men. Keep in mind that women tend to also live longer than men.

Because age seems to be associated with obesity prevalence among urbanites, it would be reasonable to look for a factor that significantly increased survival rates as one of the main reasons for the steep increase in the prevalence of obesity in the USA in the 1980s. If significantly more people were surviving beyond age 40 in the 1980s and beyond, this would help explain the steep increase in obesity prevalence. People don’t die immediately after they become obese; obesity is a “disease” that first and foremost impairs quality of life for many years before it kills.

Now look at the graph below, from an article by Armstrong and colleagues (). It shows a significant decrease in mortality from infectious diseases in the USA since 1900, reaching a minimum point between 1950 and 1960 (possibly 1955), and remaining low afterwards. (The spike in 1918 is due to the influenza pandemic.) At the same time, mortality from non-infectious diseases remains relatively stable over the same period, leading to a similar decrease in overall mortality.

When proper treatment options are not available, infectious diseases kill disproportionately at ages 15 and under (). Someone who was 15 years old in the USA in 1955 would have been 40 years old in 1980, if he or she survived. Had this person been obese, this would have been just in time to contribute to the steep increase in obesity trends in the USA. This increase would be cumulative; if this person were to live to the age of 70, he or she would be contributing to the obesity statistics up to 2010.

Americans are clearly eating more, particularly highly palatable industrialized foods whose calorie-to-nutrient ratio is high. Americans are also less physically active. But one of the fundamental reasons for the sharp increase in obesity rates in the USA since the early 1980s is that Americans have been surviving beyond age 40 in significantly greater numbers.

This is due to the success of modern medicine and public health initiatives in dealing with infectious diseases.

PS: It is important to point out that this post is not about the increase in American obesity in general over the years, but rather about the sharp increase in obesity since the early 1980s. A few alternative hypotheses have been proposed in the comments section, of which one seems to have been favored by various readers: a significant increase in consumption of linoleic acid (not to be confused with linolenic acid) since the early 1980s.

51 comments:

I'm skeptical about the noninfectious disease death rate remaining so steady from over the last century. Sure, we haven'e made major progress with cancer, but I thought we were making headway against heart disease, stroke, and chronic lower respiratory diseases, and death from diabetes.

"In the most recent period from 1969 to 2010, significant progress in the prevention, diagnosis, and treatment of cardiovascular diseases likely contributed to the 41 percent decline in age-adjusted mortality despite cancer continuing to increase from 1969 to 1990 and chronic lower respiratory diseases continuing to increase from 1969 to 1998."

Hi Steve. While modern medicine and public health initiatives have had success in dealing with infectious diseases, they have had a relatively poor record at addressing degenerative diseases. Moreover, as people live longer, more die from degenerative diseases.

Do you think there's much to the epigenetic influence caused by WWII? People who reached 40 in 1980 were born during the war and it's quite likely their mothers were highly stressed emtionally, physically and nutritionally.

Ned, thanks for the really interesting post/theory! I have to argue this statement though: "obesity is a 'disease' that first and foremost impairs quality of life for many years before it kills."

It's certainly the case that there can be disability with severe obesity (been there). However, I don't know that it is fair to say that it is in fact obesity that kills people.

True, adipose tissue is not benign, but it's not clear (to me anyways) how much of what actually kills (cancer, CVD, etc) is from how fat we are vs other things like inflammation as a result of diet and lifestyle.

I'm not a Taubes evangelist by any means, but I do like his "what makes us fat makes us sick."

Hi DancinPete. Interesting theory. The problem with, in my view, is that many populations have undergone similar stress and still avoided obesity and degenerative diseases. In some cases, even more stress; for example, the traditional Okinawans.

Hi Beth. Body fat is often highly insulin sensitive among those who gain it easily. So, gaining body fat easily, particularly subcutaneous fat, is not necessarily a sign of poor health. In fact, it may well be the opposite in some people.

Abnormal visceral fat accumulation is another story, and it indeed seems to be associated with chronic stress leading to chronically elevated cortisol levels. However, visceral fat is very easy to “mobilize” through exercise.

As for subcutaneous body fat, which is harder to mobilize, the problem seems to be when body fat cells start becoming insulin resistant, which happens at different thresholds to different people.

Pro-inflammatory hormones, such as TNF, increase in circulation together with body fat. Anti-inflammatory hormones, such as adiponectin, decrease. Hence the very high correlation between obesity and cancer rates:

I've just read "an Epidemic of Absence" which makes a similar point, in terms of infectious disease and parasite incidence being inversely associated with allergies and autoimmunity, including diabetes. The humble pinworm, for example, has become a threatened species in the USA.Junk foods are prebiotic for junk bacteria and yeasts.It's early days yet for applying the "Hygiene" and "Old Friends" hypotheses to the obesity epidemic, and I'd like to see what you make of the epidemiology in the book.It seems to me that there are substantially higher odds ratios inhygiene hypothesis epidemiology than in most diet-health research.

The age point is a good one but it still leaves a lot to explain. "Paleo" people suggest that the rise of obesity coincides with the onset of government propaganda on healthy diets, with its thrust against fat and recommendations to eat more carbohydrates. Could they be right about this coincidence in time?

Hi dearieme. If you take a look at the Austin et al. article, which is linked, they note that: “The percentage of energy from carbohydrates increased from 44.0% to 48.7%, the percentage of energy from fat decreased from 36.6% to 33.7%, and the percentage of energy from protein decreased from 16.5% to 15.7%.”

These are numbers for macronutrients, and are based on a comparison between data from NHANES I, 1971–1975 and NHANES 2005–2006. The difference in total calorie intake is not much more impressive either.

Even if there was a lot of propaganda, what matters are the changes resulting from the propaganda. And these changes are too small to fully account for the sharp increase in obesity of 11.9% to 33.4% (in men) for the same period; about the same magnitude in women.

Both childhood and age-adjusted adult obesity began increasing dramatically around 1980...and both increased appx. 2.8-fold. I don't think that an aging population is a convincing explanation on its own.

Hi Anon(2). Maybe we’ll see a leveling off from 2010 on, unless an epigenetic effect takes on from there. This would be related to severe insulin resistance among obese mothers affecting their children, leading to a dramatic increase in childhood obesity. This seems like a relatively recent phenomenon that is already happening among certain groups.

I have to think a bit more about this, but the differences in steepness for the obesity increases among adults and children in JS’s graph (http://imgur.com/Jhzsb) seem to support this blog post’s main argument.

Hi JS. By “age-adjusting” I meant something akin to “controlling” for age, which would be analogous to dividing the obesity prevalence figures by a number that would be a function of age.

The age-adjustment in the data you referred to employed a weighting approach, which is very useful when we compare different populations (see: http://en.wikipedia.org/wiki/Age-adjusted), but which had the effect of making the within-population age-adjusted numbers very similar to the non- age-adjusted ones.

Dearieme suggested that government propaganda (dietary guidelines) may have contributed to the increase in obesity that has occurred in recent decades. You responded that the changes in intake of fats, carbohydrates and proteins over the period in question were too small to have any effect.

While total fat consumption has changed little, there has been a huge change in the types of fats consumed that have contributed not only to increased obesity but to also to increased inflammation. During the past century intake of linoleum acid (LA) has increased from 1% of calories to about 8% of calories. USDA dietary guidelines advocate substituting vegetable oils for animal fats and restricting intake of animal fats. Vegetable oils have supplanted lard for frying in fast foods joints. Since 1980 intake of vegetable fats high in LA has increased by 43% while there was a corresponding decrease in consumption of animal fats.

LA is the precursor for arachidonic acid (AA) which is the backbone of both endocannabinoids anandamide (which name is derived from ancient word anada meaning bliss) and 2-arachiindonoylglycerol (2-AG) which activate the same receptors activated by marijuana. For convenience I will efer to endocannabinioids as “bliss factors” It has been found that excessive dietary intake of LA causes hyperactivity of the bliss factors that leads to increased food intake and obesity.

A recent study in the Netherlands fed rats from 1% to 8% of calories as LA which corresponds to the increase in LA intake that has occurred in the US. The higher LA intake caused a threefold increase in the bliss factors which stimulated appetite and led to obesity in rats fed 8% LA. The adverse effect of excessive LA intake was reversed by feeding the rats omega-3 fats.-

It is apparent that increased LA intake is a major, if not the primary, cause of increased obesity in the U.S. LA is also highly inflammatory and contributes to increased risk of many diseases.

@Jack C: that's an interesting one. Lately I've taken to saying that what needs explanation is the way that people keep on eating, and have speculated that some unidentified infection has been suppressing the satiety response. Your suggestion is more direct - food has become more fun and so people munch on.

Can you cure my ignorance: are all vegetable oils a menace in this regard, even the blessed olive oil?

Hi Jack C. Indeed, I thought about LA intake as possibly THE main cause. I changed my mind after I looked into calorie intake numbers. Based on the mechanism you described in your comment, if LA intake was the main cause of the sharp increase in obesity since the 1980s, shouldn’t we have seen also a more marked increase in total calorie intake starting in the 1980s?

Note that in my response to dearieme’s comment I also indicated that: “The difference in total calorie intake is not much more impressive either.” This is based on the data, which I discussed in part in the post – here is a relevant quote from the post for easy reference:

“The differences in calorie intake and macronutrient composition are simply not large enough to fully account for such a steep increase. And the data is actually full of oddities. For example, an article by Austin and colleagues (which ironically blames calorie consumption for the obesity epidemic) suggests that obese men in a NHANES (2005–2006) sample consumed only 2.2 percent more calories per day on average than normal weight men in a NHANES I (1971–1975) sample”.

Olive oil has only 10% linoleic acid (as George Henderson said) so it is not a problem. Furthermore, olive oil is expensive so it is not widely used in processed foods.

Soybean oil now accounts for more than 80% of vegetable oil consumption. Production of soybean oil tripled between 1970 and 2005. You will find soybean oil in a great percentage of processed foods such as bakery products, corn chips, soups and most everything else. Furthermore, it is cheap and soy chow is used for feeding cattle, chickens, pigs and milk cows and as a result the LA content of eggs, meat, milk, butter and cheese is higher and omega-3 fats lower than it would be if the animals were fed their natural diets.

In response to the suggestion that LA intake was the main cause of the sharp increase in obesity since the 1980’s, you noted that if that were so we should have seen a marked increase in total calorie intake starting in the 1980’s.

Good point and I did ponder that before making my comment. I can think of two possible reasons why the data does not show a marked calorie increase associated with the increase in obesity: First, it is possible that the historical calorie intake data is not accurate. Second, there may have been a decrease in thermo-genesis due to increased intake of LA. It has long been known that intake in omega-3 fats can cause an increase in thermo-genesis that will reduce fat accumulation. Excessive intake of LA perhaps may cause a decrease in burning of fat that leads to weight gain. Excessive intake of LA does increase inflammation which reduces lipoprotein lipase which causes an increase in TG due to reduced burning of fat. This scenario seems a possibility.

I erroneously stated that the study on the relation ship between LA and obesity was done in the Netherlands when in fact it was done in Norway. The Pubmed ID of the study, which has free full text, is 22334255.

The very strong correlation between poultry intake and obesity was a surprise to me even though I know that LA intake of poultry is about 18%. It would be interesting to know how much of the LA in poultry came from the frying.

Another point of interest from the study: The classic method of making the animals obese is to feed them 60% fat of which 8% is LA. It was found that if the LA in the diet of rats is reduced to 1%, a diet of 60% fat does not make the rats obese.

On calorie intake and obesity: consider a full-grown adult male, previously having a steady weight. How many extra calories per year are needed for him to put on ten pounds per year, assuming that his energy expenditure doesn't change? What are those extra calories as a percentage of his previous annual intake?

"Wouldn't you say that this is a relatively recent phenomenon though?"

Nope: "The percentage of children aged 6–11 years in the United States who were obese increased from 7% in 1980 to nearly 20% in 2008. Similarly, the percentage of adolescents aged 12–19 years who were obese increased from 5% to 18% over the same period."

I'm going with the linoleic acid hypothesis, myself.

I think the increase in childhood obesity during a period when childhood mortality did not change by any meaningful amount torpedoes this theory...

Remnant has left a new comment on your post "The steep obesity increase in the USA in the 1980s...":

You might consider adding an ethnic breakdown to the data, which might partially account for the increase: the period since 1965 - and particularly since the 1980s -- has seen a vast increase in the number of Latin American hispanics in the country. They tend to have high obesity rates, which could be a contributing factor to the data. Increases in the African-American population may also contribute as their obesity rates are the highest of any major ethnic group.

I actually like the LA connection hypothesis, but wonder if it can fully explain the sharp increase. Here is the problem. The sharp increase since the 1980s is difficult to reconcile with any factor that might have had a gradual effect.

Unless one is to believe that LA consumption had an almost binary increase around 1980, with an immediate negative effect, it is hard to buy into it. (An alternative version of this theory would be a sharp increase in LA consumption a few years before, with a lagged binary effect – still, not likely.)

The same problem applies to the immigration hypothesis, assuming that immigrants were not obese upon arrival – a reasonable assumption, from what I can observe living on the Mexico-USA border. I’d suspect that obesity is more common in descendants of immigrants.

As for the increase in childhood obesity, it has been brought up by JS in a previous comment above (see graph linked below). The increase is a lot less steep than for adults – in terms of percentage points, about half. But indeed, there is clearly a significant change in childhood obesity around 1980.

http://imgur.com/Jhzsb

Since childhood obesity covers a good age range – 2 to 19, the change may be due to prenatal exposure, something that I mentioned in a previous comment above, which would make it fairly consistent (I think) with the main idea behind this post.

Prenatal exposure to an abnormal environment – in terms of hormones, glucose etc. – creates a vicious circle that is very hard to break away from.

It is important to point out that this post is not about the increase in obesity in general, but rather about the sharp increase in obesity since the 1980s.

Still, I think that several of the possible theories being discussed here are interesting. I will revise the post, adding a “PS” note, including one of the possible theories that seems to be favored (LA), raised in this comments section, which could explain the phenomenon.

Keep them coming!

What we have seen since the early 1980s could be a combination of multiple factors that, when operating together, have an effect that is much sharper than if the factors were operating alone.

While there are many factors that have contributed to the increase in obesity that has occurred since 1980, it appears that the dramatic increase in LA is the primary factor because arachidonic acid (AA), which is derived from LA, is the backbone of the endocannabinoids that activate the same receptors that are activated by marijuana.

Endocannabinoids are lipid mediators that increase appetite AND will increase the synthesis of fat by the liver even when there is no increase in intake of calories! Thus the increase in obesity can occur in association with a very modest increase in calories. It appears that the increase in LA intake provides "a unifying theory of obesity".

http://www.ncbi.nlm.nih.gov/pubmed/22334255

Calcium deficiency causes an increase in calcitriol and consequent inflammation which results in increased lipid synthesis. The decrease in intake of dairy products that has occurred since 1980 could also contribute in a small way to increased obesity.

As you can see from my comments above, I am open to but somewhat skeptical of the idea that omega-6 fat consumption explains the sharp increase in obesity since the 1980s. As it turns out, my next post will provide an example that challenges this view – i.e., support my skepticism. Stay tuned!

And, of course, there are the other two popular contenders: increased BPA accumulation, and changes in the American gut flora.

I have serious doubts about the BPA hypothesis, but some aspects of it are plausible.

Intestinal ecology, on the other hand, seems to be accumulating a great deal of evidence. But our internal microbial ecology is affected by many things, including antibiotics (whether deliberately administered or from industrial foods), as well as dietary composition. This makes it not so much a competing hypothesis to dietary hypotheses as another dimension to them.

I'm afraid I think obesity is quite multifactorial, no matter how much biomedical researchers would like to find a single culprit.

From all said it looks most probable that the dominant cause are antibiotics and less dominant causes may be industrial toxins like MSG.

Since increase is paralleled in both adults and children I doubt its about other drugs - most drugs are usually not given to infants as of adverse effects, but antibiotics are fairly regular and overprescribed (children suffer around 6 respiratory infections per year and most of them have otitis at least once during first year of life).

In combination with modern industrial toxins (like MSG, BPA) and higher usage of all forms of sugar, there is probable synergy to obesity pathway of these various factors. Nutrient deficiencies also add to this, particularly that of retynol.

In addition to increases in LA consumption, the early '80's is also a time of increasing trans fats consumption. It was in 1983 that Mcdonalds, at the urging of the govt, switched from beef tallow to trans-fats for frying. I expect almost the entire fast food industry followed shortly thereafter.The same trans fats found their way into most processed foods.

The 80's was also when HFCS started to replace sugar.

The obesity changes in kids are interesting, as they are not medicated as much as everyone else. But the kids today are born of people who have been eating all this stuff for at least a decade before having their kids - epigenetic changes being passed on?

Obesity in the United States has been increasingly cited as a major health issue in recent decades. While many industrialized countries have experienced similar increases, obesity rates in the United States are among the highest in the world.Of all countries, the United States has the highest rate of obesity. From 13% obesity in 1962, estimates have steadily increased, reaching 19.4% in 1997, 24.5% in 2004 26.6% in 2007, and 33.8% (adults) and 17% (children) in 2008. In 2010, the CDC reported higher numbers once more, counting 35.7% of American adults as obese, and 00M-657, 000-318, 000-283 17% of American children.

Your blog is really insightful! Looking at your work has enlightened me. I discovered a lot from it. I will take a note of your site and will pursue to go through your forthcoming blog posts. Wonderful! Thanks a lot!

Ned Kock

About Me

I strongly believe that lifestyle, nutrition and exercise habits that are compatible with our evolutionary past are the key to optimal health. On the other hand, I do not believe that closely mimicking life in the Paleolithic is optimal for health, or even viable. I am a researcher, software developer, consultant, and college professor. Two of my main areas of research are nonlinear variance-based structural equation modeling, and evolutionary biology as it applies to the study of human-technology interaction. My degrees are in engineering (B.E.E.), computer science (M.S.), and business (Ph.D.). I am interested in the application of science, statistics, and technology to the understanding of human health and behavior. I blog about evolution, health, statistics, and technology. My personal web site contains links to my contact information and freely available articles related to the topics of my blogs: nedkock.com.

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